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RACP Written > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

What is the presentation for nephritic syndrome?

A

Haematuria, proteinura (<200), hypertension, renal impairment, peripheral oedema

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2
Q

What are the 3 types of nephritic syndrome?

A

Post-strep GN
Chronic GN (FSGS, MPGN, membranous GN, IgA N, SLE, HSP)
RPGN (cresenteric)

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3
Q

What do the complement levels do in post-strep GN?

A

Low C3, NORMAL C4 (Strep is 3x more dangerous)

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4
Q

What do the C3 and C4 levels do in MPGN?

A

PERSISTENLY LOW C3. BUT ALSO LOW C3 and C4 to start with

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5
Q

What conditions causing nephritis will have low C3 and C4?

A

MPGN, shunt nephritis, SLE

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6
Q

What is the most common cause of nephritic syndrome?

A

IgA nephropathy (different to IgA vasculitis ie HSP. Most common type of vasculitis in children)- post infection

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7
Q

What is the treatment for IgA nephropathy?

A

Immunosuppression, needs atleast 6 months of steroids.
ACEI for persistent proteinuria

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8
Q

What conditions have a NORMAL complement in nephritis?

A

FSGS, IgA nephropathy, HSP, ANCA, HUS, ALports (alports has SSNL)

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9
Q

How do you calculate the FENa?

A

URINE Na x serum Cr x 100
DIVIDED BY
PLASMA sodium x urine Crr ratio

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10
Q

How much should your BP dip by overnight?

A

10%

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11
Q

Anterior lenticonus is pathognomonic of which suyndrome

A

Alports.
Present in 30%

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12
Q

What is a risk of NF in relation to the kidneys

A

Renal artery stenossi

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13
Q

What are the three embryological origins of the kidney

A

Pronephros
Mesonephros - functioning kidney until week 10. Helps form ureters and bladder, later becomes gonads
Metanephros - this form the actual kidney

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14
Q

What structure forms the foetal kidney and what time in the embryological period is this

A

Mesonephros
Weeks 5-10

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15
Q

What structures forms ACTUAL kidney

A

Metanephros
MET criteria for actual kidney

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16
Q

When does the pronephros appear

A

4 weeks

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17
Q

When does renal development stop in the embryogenic period

A

36 weeks OR 4 weeks postnatal period which ever comes first

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18
Q

When does the amniotic fluid become predominantly urine

A

15 weeks
Before that, 2/3 urine and 1/3 pulmonary fluid

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19
Q

Does anhydromnios always mean renal dysfn

A

No, can be invivo placental dialysis, these kids will have normal renal funtion in later life

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20
Q

AT birth, what is the GFR % compared to adult and when does the GFR reach adult values

A

5% at birth, takes 2 years to reach adult levels

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21
Q

What is normal FENa (%)

A

1%

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22
Q

Why do premature infants have a high FENa

A

Premature kidneys so often need sodium supplementation to avoid hyponatraemia

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23
Q

Between what time frame is there a rapid increase in GFR post birt

A

First 4 days

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24
Q

HOw long does it take for the GFR to double post birth

A

2 weeks.
2x by 2 weeks

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25
Q

What is the most metabolic part of the kidney

A

PCT

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26
Q

What is the name of the transporter responsible for Na reabs in PCT

A

Na-K ATPase-active transporter

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27
Q

What is resorbed in the PCT

A

Na, Bicarb, Phos, Glu, Ca (basically everything ex Mg which is MOSTLY absorbed in LOH)

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28
Q

What is Fanconi syndrome

A

Proximal tubule dysfn- phophaturia, glucosuria, hypouricaemia, amonoaciduria

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29
Q

Clinical presentation of Fanconi syndrome

A

FTT, polyuria, polydipsia, dehydration, constipation, ricketts.

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30
Q

Most common genetic cause of Fanconi syndrome

A

Cystinosis

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31
Q

What type of RTA does Fanconi syndrome present with

A

Type 2 RTA- proximal. HCO3 wasting.

Fanconi is TWICE as worse.

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32
Q

Main function of Loop of Henle

A

Na, Ca, Mg and K resorption

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33
Q

How is sodium resorbed in the loop of Henel

A

Na K Cl2 transporter

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34
Q

Where do loop diuretics bind and how does it change BP

A

Bind and INHIBIT Cl on the NAKCL2 transporter, means no Na resorbed and so no water resorbed.
In Barter’s there is an inborn error of metabolism in the Cl part of this channel

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35
Q

How is Na resorbed in the distal tubule

A

Na Cl co-transporter

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36
Q

Where is the main site of aldosterone action

A

collecting tubule and then DCT

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37
Q

Where is Gitelmann syndrome affected

A

DCT

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38
Q

What does Aldosterone do in the Collecting tubule

A

increase ENaC and NaK ATPase activity to increase water and Na resorption

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39
Q

How does Spiro work

A

Blocks aldosteroner receptors so CANNOT increase ENAC and NaK ATPase to increase water resorp. K sparing.

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40
Q

What does ADH do in the colleting duct

A

Increase release of Aquaporin from the vesicles to increase water resorption

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41
Q

What releases renin

A

Juxtaglomerular appratus

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42
Q

What are the triggers for renin release

A

THINK END GOAL IS TO RESORB WATER.
Stretch receptors (Reduced in afferent), baroreceptors and sympathetic activity, increased solute load

Ahhhhhh = sounds of a nice stretch= afferent

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43
Q

Name the pathway of renin-angiotensin-aldosterone system

A

REnin from juxtaglomerular apparatus activates angiotensin (from liver) to angiotensin I which –> Angiotensin II with ACE.
This causes systemic vasoconstriction and increase aldosterone release.

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44
Q

What is Conns syndrome

A

primary hyPER aldosteronism- so hypertension, raised ECF volume expansion and renin suppression

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45
Q

What is Liddle syndrome

A

AD disorder- gain of function in ENAC Channel
increased sodium and water resorption but renin AND also suppressed on bloods

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46
Q

Treatment for Liddle syndrome

A

Amiloride- blocks ENaC channels

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47
Q

What medication blocks ENAc channels

A

Amiloride

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48
Q

What cells repease EPO

A

Peritubular cells in the renal cortex
INTERSTITIAL FIBROBLASTS.

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49
Q

Action of 1-hydroxylase

A

Convert 25-OHVitD to 1,25-OHVit D

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50
Q

What gives a false neg in terms of haematuria

A

Vit C/ascorbic acid

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51
Q

Are nitrites specific or sensitive for UTI

A

Specific

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52
Q

What scan is good for VUR

A

MCUG- dye from the bladder UP
Also good for posterior urethral valves

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53
Q

What is DMSA scan good for?

A

STATIC scan- just a picture.
Good for UTI, ectopic or duplex kidney

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54
Q

What is MAG3 good for

A

Dynamic scan- isotope filtered from kidneys down to bladder. Good for upper urinary tract obstruction.

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55
Q

Most common cause of CKD in kids?

A

CAKUT

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56
Q

What does a PUJ obstruction lead to ? And what is a scan used for further assessment for this?

A

Hydronephrosis
MAG 3- REMEMEBER UPPER TRACT PROBLEMS

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57
Q

What shows up on a DMSA scan for multicystic dysplastic kidney

A

No functioning kidney

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58
Q

What are associations of Horseshoe kidney

A

Turners
Trisomy 21
VACTERYK
Fanconi Anaemia

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59
Q

What surgical procedure should NOT be performed in babies with hypospadias

A

circumscision

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60
Q

3 common examination findings of testicular torsion

A

horizontal lie, loss of cremasteric reflex and diffuse tenderness

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61
Q

Where is the pain in torsion of hyatid of Morgagni

A

Upper pole of testes, common in prepubertal age

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62
Q

Name 5 genetic causes of Fanconi syndrome

A
  1. Cystonosis
  2. Galactossemia
  3. Tyrosinaemia
  4. Hereditary fructose intolerance
    5.- Glycogen storage disease
  5. Lowes syndrome
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63
Q

What is Lowe’s syndrome

A

Mental retardation
Reduced tone
renal dysfn

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64
Q

What type of disorder is CYtininsos

A

Glycogen storage disorder- defect in gene that codes for cystine transport protein.

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65
Q

Difference between cystinosis and cystinuria

A

Cystinuria= defect in reabs of and hence excessive excretion of amino acids = recurrent stone formation.

Cystinosis= defect in carrier –> deposition in eyes, kidneys etc

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66
Q

Where is the problem in x linked hypophos rickets

A

In PCT- prob with reabs of phosphate

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67
Q

Electrolyte abnormalities in Barters syndrome

A

Low Cl
Low K
Mg, Ca and Na may also be low

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68
Q

What is in the urine for Barters

A

INAPPROPRIATELY HIGH urine Cl and NA. Also calcium.

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69
Q

Difference between pseudo and actual Barters?

A

Pseudo will have appropriately low urine Cl and Na

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70
Q

What can cause pseudo Barters

A

THINK LOW Cl
- congenital chloride diarrhoea
- CF
- laxative abuse

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71
Q

Which drug/class of drugs have the same effect as Barters

A

Loop diuretics ie Frusemide

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72
Q

Differentials of HYPOkalemic, HYPOchloremic metabolic alkalosis in kids

A
  1. Surreptious vomiintg (hidden)
  2. Laxative abuse/ Congenital Cl losign diarhoea
  3. Diuretic abuse
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73
Q

The epithelial sodium channel in the collecting duct is regulated by what? (past question)

A

ENaC
Aldosterone.

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74
Q

What does Gittelmans present with

A

Hypokalemia
Met alkalsois
Hypomagnesemia
HyPOcalciuria

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75
Q

What is the location of Type 1 bs Type 2 RTA

A

Keep 2 things closer so Type 2 is proximal and type 1 is distal

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76
Q

Which RTA has low bicarb

A

Type 1 (Distal) BUT proximal harder to treat so supplement with bicarb

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77
Q

Features of Type 1 RTA- clinical

A

Nephrocalcinosis, faltering growth, severe hypokalemia

78
Q

What condition can trimethoprim and toulene (glue) cause

A

Type 1 RTA

79
Q

Main defect in type 1 RTA

A

Failure of H+ excretion so no bicarb abs

80
Q

Which condition has idiopathic hypercalcemia of infancy

A

Williams syndome

81
Q

What do symptomatic renal cysts present wit

A

Symptomatic simple renal cysts may present with loin pain, haematuria, or recurrent UTI.

82
Q

What is the most common outcome of a MCDK in the long term

A

Normal renal function (overall)

83
Q

What are some common complicatiosn of MCDK

A

15% have contralateral VUR
5-10% have contralateral hydronephrosis
0.2-1.2% develop hypertension
0.3% risk of Wilms

84
Q

How much %body weight is water in preterm vs term babies

A

85% in preterm
80% in term

85
Q

What is a safe rate of correction for hyponatraemia

A

1mmol/4 hours
Total 6-8mmol/24 hours

86
Q

In conditions with hyPOkalemia, what happens to Cl in urine

A

LOW to compensate. To do with the transporters.

87
Q

Medication to treat hyperkalemia - the most important

A

Calcium gluconate- stabilise myocardium

88
Q

Medication to treat hyperkalemia post stabilisation of myocardium

A

insulin-dex
salbutamol
dialyssi

89
Q

4 main symptoms of hyPOcalcaemia

A

Tetany, paresthetias, muscle cramps, seizures

90
Q

Main symptoms of HyPERcalcaemia

A

Moans, groans, bones and stones
Headache, constipation, lethargy, renal stones, hallucinations

91
Q

What is more accurate when testing for protein loss- PCR or ACR

A

PCR more accurate (think PCR more accurate in COVID)

92
Q

What is the most common cause of proteinuria in kids

A

Benign orthostatic proteinuria

93
Q

Which nephritic syndromes are caused by type 3 hypersensitivity reactions

A

IgA nephropathy
Post-strep GN

94
Q

Which nephritic syndrome is caused by type 2 hypersensitivity reactions

A

Goodpastures

95
Q

What is the definition of nephritic range proteinuria

A

> 200g/L

96
Q

What are the three types of RPGN

A

Goodpastures- type 2
ANCA associated GPA or microscopic polyangitis

97
Q

Which RPGN has upper airway involvement

A

GPA or any ANCA associated vasculitis
(pulmonary renal syndrome)

98
Q

Name the disease:
Recent sore throat. Low C3

A

PSGN

99
Q

Recent illness weeks ago. Spots on back of legs and buttocks. Joint pain.

A

HSP

100
Q

Haemturia post URTI

A

Ig A nephropathy

101
Q

Pulmonary renal syndrome associated with what autoimmune marker?
Hint think of a disease that affects both

A

ANCA associated

102
Q

Persistently low C3

A

Membranioproliferative

103
Q

Most common nephrotic syndrome

A

Minimal change

Nephrotic does not care about change.

104
Q

3 diagnostic crteria for nephrotic syndrome

A

Proteinuria (>200), hypoalbuminaemia and oedema

105
Q

Age for atypical nephrotic syndrome

A

<18months or >12yo

106
Q

What is the definition of remission in nephrotic syndrome

A

> 3 days of no proteinuria

107
Q

Treatment for nephrotic? (First line)

A

Steroids: 60mg/m2 for one month with prophylactic antibiotics

108
Q

Treatment for frequently relapsing nephrotic syndrome

A

Calcineurin inhibitor- Cyclosporin or Tacro. Tacro more fabourable

109
Q

What class of drugs is Tacrolimus

A

Calcineurin inhibitors

110
Q

What is the natural history of nephrotic syndromes

A

Gets better once you hit puberty

111
Q

What % of kids respond to steroids in nephrotic syndrome

A

90%

112
Q

What % of kids will have a relapse in nephrotic

A

75%

113
Q

What percentage of kids will have multiple relapses in nephrotic

A

50%

114
Q

What subset of kids with nephrotic are most likely to grow out of their nephrotic syndromes- ie the name given to this group

A

Steroid sensitive

115
Q

What are known complications of nephrotic syndrome (name 5)

A

Thrombosis (saggital sinuts thrombosis), Vit D def, hypothyroidism, raised chol, infection (due to oedema)

116
Q

Dilatation of the afferent glomerular arteriole to maintain GFR during times of hypotension, is mediated by which of the following?

A

PGE2

117
Q

What medication is an absolute contraindication in phaechromocytoma?

A

Beta blockers. Because unopposed alpha action which can cause MI and brain bleeds.

118
Q

What is the most appropriate dietary management to reduce renal stones

A

reduce sodium

119
Q

In nephrotic syndrome hypercoagulability is due to deficiency of

A

Antihrombin 3

120
Q

Growth hormone is used in chronic renal disease. What is the mechanism of GH deficiency in chronic renal disease?

A

GH resistance

121
Q

Haemofiltration is a process best described by

A

ULTRAFILTRATION
remember peritoneal dialysis= osmotic pressure

122
Q

What is the medication used for raised acute HTN causing neurovascular changes ie PRESS

A

Sodium nitroprusside is a medication used in the management of acute hypertension. It is a potent vasodilator and is administered as an IV infusion with intensive monitoring in place

123
Q

Primary mechanism leading to oedema in nephrotic syndrome

A

Reduced capillary oncotic pressur

124
Q

Relationship between Angiotensin II and Na?

A

In the proximal convoluted tubule of the kidney, angiotensin II acts to increase Na-H exchange, increasing sodium reabsorption. Increased levels of Na in the body act to increase the osmolarity of the blood, leading to a shift of fluid into the blood volume and extracellular space (ECF).

125
Q

What forms the collectinf systems of the kidneys

A

Ureteric bud

126
Q

What mediates renal efferent vasoconstriction

A

Angiotensin II

127
Q

What is primarily activated in PSGN (ie which complement pathway)

A

ALternate pathway
Remember only C3 low

128
Q

Treatment for hypocalcaemia in an ED setting.

A

Ca gluconate

129
Q

What should you correct first, hypocalcaemia or acidosis

A

Acidosis as Calcium depends on pH

130
Q

What values of FENa determine pre-renal vs renal cause of AKI

A

<1%= pre-renal
>2%= ATN

131
Q

Name 5 complications of AKI

A

Acidosis
Hyperkalemia
Hypocalcemia
Severe symptomatic uraemia
Fluid overload

132
Q

What happens to ADAMS T13 in HUS

A

LOW

133
Q

Most common cause of CKD in kids (1 and 2)

A
  1. CAKUT
  2. Chronic glomerulonephritis
134
Q

What are indications to start dialysis

A

Hyperkalemia - refractory to treatment
Uremia
Drug OD ie vanc/gentamyxin
Fluid overload
Acidosis
High phosphate

135
Q

Name what grade VUR this is.
Reflux into non dilated ureter

A

Grade 1 (pic in notes)

136
Q

Name what grade VUR this is.
Into pelvis and calyces without dilatation

A

Grade 2

137
Q

Mild to mod dilatation of ureter, renal pelvis and calyces with minimal blutning of the fornices

A

Grade 3

138
Q

Moderate ureteral tortuosity and dilatation of the pelvis and calyces

A

Grade 4

139
Q

Gross dilatation of the ureter, pelvis and calyces with loss of papillary impressions and ureteral tortuosity

A

Grade 5 VUR

140
Q

In kids with UTI, who should have an ultrasound prior to discharge

A

Seriously unwell children, those with renal impairment, and boys <3 months of age should have a renal ultrasound prior to discharge

141
Q

Who should get non-urgent renal ultrasounds post UTI

A

Only kids with recurrent UTIs

142
Q

What two virus can cause cystitis

A

Adenovirus and Influenza

143
Q

When do most children become dry in the day vs at night

A

At night- 6-9 months and daytime bu 3 years

144
Q

Definition of primary nocturnal eneursis

A

Never achievement night time dryness

145
Q

What is the most common cause of daytime voiding disorder

A

Overactive bladder and URGE = most common symptom

146
Q

What is the expected bladder capacity

A

(age+1) x 30 mls

147
Q

When should Desmopressin be used in nocturnal eneurisis

A

FOr special situations ie sleepover.
Only good for short term

148
Q

What is the medication for detrusor instability

A

Oxybutynin
(anti-cholinergic)

149
Q

Classic presentation of voiding postponement

A

Delay going to the toilet when participating in activities/at school etc –> overflow incontinence.

150
Q

Classic presentation of underactive bladder

A

Decreased voiding frequency secondary to neurological causes ie sacral agenesis, bladderoutlet obstruction. Need to optimise bladder emptying and pelvic floor relaxation

151
Q

What is dysfunctional voiding

A

Incomplete relaxation of pelvic floor muscles and during bladder emptying

152
Q

What is vaginal reflux

A

Entrapment of urine by labia because of poor posture/entrapment by thighs (overweight).
Leads to wetting after voiding/standing up/physical activities when trapped urine leaks out.

153
Q

What is giggle incontinence

A

Rare often hereditary. Involuntary complete ballder emptying on laughing with otherwise normal bladder and bowel function

154
Q

What is extraordinatory day time frequency incontinence

A

Isolated sudden frequent voiding of small volumes without nocturia, atleast 1/hour. Usuaull self limited. Can try anticholinergic.

155
Q

What condition:
Flank mass and HTN

A

Wilms

156
Q

What condition:
Cafe au lait and HTN

A

NF1 - assocaited with renal artery stenosis

157
Q

What condition:
Tachycardia, flushed, HTN

A

Phaechromocytoma

158
Q

Which is worse, aut recessive or dominant PKD

A

RECESSIVE

159
Q

US findings for ARPKD

A

large, echobright kidneys. Wont see true cysts

160
Q

What other condition is ALWAYS associated with ARPKD

A

Hepatic fibrosis

161
Q

What other condition is ALWAYS associated with ARPKD

A

Hepatic fibrosis

162
Q

Gene for ARPKD vs ADPKD

A

PKHD1 mutation
6 for recessive

PKD1
16 for dominant
(Dominant larger)

163
Q

US for ADPKD

A

Discrete cysts

164
Q

Classic appearnce of MCDK

A

multiple non communicating cysts with non functioning renal parenchyma- only one sided.
Should always monitor other kidney

165
Q

Main cause of nephrocalcinosis

A

Distal RTA - remember thats type 1 RTA

166
Q

3 other causes of nephrocalcinosis

A

Ex-prem neonates
Vit D treatment for hypophosphataemic rickets
oxalosis

167
Q

Most common renal stone type

A

Calcium oxalate

168
Q

Most common kidney stone disorder?

A

Cystinuria (NOT CYSTINOSIS)
Defect in renal reabs of cystine

169
Q

Mechanism of action of acetazolamide

A

Acetazolamide= Carbonic ANHYDRASE inhibitor
Prevents reabs of sodium and bicarb

170
Q

What does Dopamine do to afferent and efferent arterioles

A

DILATATION OF BOTH.
Increased renal blood flow to both but no increase in GFR

171
Q

What is Dent Disease
Thing about going to the dentist.

A

Dent disease is a rare genetic kidney disorder characterized by spillage of small proteins in the urine, increased levels of calcium in the urine, kidney calcifications (nephrocalcinosis), recurrent episodes of kidney stones (nephrolithiasis) and chronic kidney disease. Dent disease affects males almost exclusively.

There is a guy driving a car who has kidney stones and calcifications due to high Ca, DENTs his car and results in leaky protein post.

172
Q

What is medullary sponge kidney disease

A

Medullary Sponge Kidney is a rare disorder characterized by the formation of cystic malformations in the collecting ducts and the tubular structures within the kidneys (tubules) that collect urine. One or both kidneys may be affected. The initial symptoms of this disorder may include blood in the urine (hematuria), calcium stone formation in the kidneys (nephrolithiasis) or infection. The exact cause of Medullary Sponge Kidney is not known.

173
Q

Common presentation of uraemia or CKD in kids

A

Vomiting

174
Q

How to calculate anion gap

A

Positive- negative
K+Na - Cl+HCO3-

175
Q

First and second largest site for NA reabs

A
  1. PCT
  2. Thick ascending loop of Henle
176
Q

Meds causing Fanconi syndrome

A

Aminoglycoside, vlaproatem cisplatin, ifosfamide
(think of the onc drugs causing nephropathy)

177
Q

Which RTA has risk of hypercalcemia and stones

A

Type 1 RTA
TYpe 1 NUMBER 1 cause of hypercalcemia

178
Q

What is type 4 RTA

A

HyPOaldosteronism

179
Q

What happens to K in Type 1, 2 and 4 RTA

A

Type 1 and 2: LOW
Type 4: HIGH

180
Q

Triggers for aldosterone release

A

Angiotensin II
Hyperkalemia

181
Q

Which condition- barter or gitelmans has hypomagnesemia?

A

GIttelMan - Low Magnesium
Barters has high ruinary cl and nephrocalcinosis due to calciuria

182
Q

Which medication does Gittelman replicate

A

thiazide diuretic

183
Q

What medication used for intracranial HTN causes hypercalciuria

A

Acetazolamide

184
Q

What is the term given to this presentation in the setting of prev nephrotic syndrome?
3 consecutive early morning urine samples with 3+ protein

A

Relapse

185
Q

What is the term given to this presentation?
Initially responsive to steroids but 2 relapses in 6 months of initial response

A

Frequently relapsing nephrotic

186
Q

What is the term given to this presentation?
Relapsing nephrotic while on steroids

A

Steroid dependency

187
Q

What is the term given to this presentation?
No response after 4 weeks of steroid therapy

A

Steroid non-responder or steroid resistant

188
Q

First and second mot common type of Nephrotic syndrome

A
  1. Minimal change
  2. FSGS
189
Q

Juvenile arthritis associated with increased symptomatic uveitis

A

Enthesitis related arthritis

190
Q

Difference between Cytinosis and Cytinuria

A

Both have high cystiene but cytinuria= secretion in urine from cystinuria and cystiene deposition in cystinosis.

191
Q

Where or what is the main problem in Cystienosis

A

Problem with cystiene transporter leading to accumulation. That’s why deposition EVERYWHERE rather than just renal stones in cystinuria.

192
Q

Which one causes Fanconi syndrome?
Cytinosis or Cystinuria

A

Cystinosis

RACP Written (18 decks)

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